&lt;p&gt;Key Genes And Pathways Controlled By E2F1 In Human Castration-Resistant Prostate Cancer Cells&lt;/p&gt;

Zhou, Qingniao; Wang, Chengbang; Zhu, Yuanyuan; Wu, Qunying; Jiang, Yonghua; Huang, Yuanjie; Hu, Yanling

doi:10.2147/ott.s217347

Cited by 11 publications

(13 citation statements)

References 67 publications

(62 reference statements)

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“…Similarly, knockout of CREB in PC3 cells resulted in reduced xenograft tumorigenicity in nude mice. We and others have previously demonstrated that TFDP3 is highly expressed in prostate cancer tissues, and not expressed or lowly expressed in normal tissues (2). TFDP3 inhibits the DNA binding, E2F1 transactivation and E2F1-dependent apoptosis (2,6).…”

Section: Discussionmentioning

confidence: 85%

“…E2F1 can regulate a large number of genes involved in diverse cellular processes, such as replication, apoptosis, checkpoint control, and DNA repair (21). We previously demonstrated that E2F1 could regulate the expression of TFDP3, while TFDP3 could negatively regulate E2F1 by inhibiting DNA binding and E2F1 transactivation (2). Hence, the binding of CREB/TFDP3 and upregulation of CREB may inhibit E2F1-dependent apoptosis by enhancing the activity of TFDP3.…”

Section: Discussionmentioning

confidence: 99%

“…In our previous study, we demonstrated that TFDP3 was highly expressed in approximately 62.3% of all stages of prostate cancer. In addition, it was broadly expressed and corresponded with E2F1 levels (2). By inhibiting E2F1 activity, TFDP3 suppressed E2F1mediated apoptosis and promoted the proliferation and tumorigenesis of PCa (2).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…The E2F1 protein (E2F1) is a transcription factor that is involved in the cell cycle, replication, and apoptosis (2). E2F1 was identified as an essential target gene that could regulate the transcription of target genes in CRPC (2). In addition, the deregulation of E2F activity and early cell cycle progression has been implicated in aggressive prostate cancer (3,4).…”

Section: Introductionmentioning

confidence: 99%

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CREB-TFDP3 Promotes Prostate Carcinoma Cell Growth by Inhibiting E2F1-Dependent Apoptosis

Li¹,

Liu²,

An³

et al. 2020

Preprint

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BackgroundThe cAMP-responsive element-binding protein (CREB) is a transcription factor that controls cell differentiation and survival. CREB is overexpressed and constitutively phosphorylated in several human cancers, including prostate cancer (PCa). However, the regulation of CREB in PCa remains to be deciphered. We previously demonstrated that TFDP3 negatively regulates E2F1 transactivation, which is important in PCa carcinogenesis. And 5 CREB binding sites were found in the upstream of TFDP3 promoter.MethodsLuciferase and chromatin immunoprecipitation assays were used to determine the association between CREB and TFDP3. Immunohistochemical staining and immuno-cytofluorescence assays were performed to determine the expression of CREB and TFDP3 in a prostate cancer tissue microarray and cell lines. Cell lines stably expressing the wild-type, overexpression or knockout of CREB and TFDP3 were established. The protein expression of CREB and TFDP3 were detected by western blot analysis. CCK-8, TUNEL staining and cell cycle analysis were used to analyze the proliferation and apoptosis of the stable cell lines in vitro. The tumor growths were evaluated using nude mice xenograft models.ResultsOur results demonstrated that CREB could bind to the TFDP3 promoter and induce the transcription of TFDP3. Both CREB and TFDP3 were highly expressed in the androgen-independent cell line PC3 and prostate cancer tissues. Furthermore, in vitro and in vivo assays demonstrated that overexpression of CREB could promote cell proliferation and inhibit apoptosis in PC3 cell lines as determined using cell CCK-8 assays, flow cytometry, and western blotting assays. Knockout of CREB in PC3 cells resulted in a reduction in tumorigenicity in nude mouse xenograft models. Notably, the overexpression of CREB/TFDP3 in the LNCap cell line increased the progression of G1 cells to S phase, while knockout of CREB/TFDP3 arrested LNCaP AI+F cells at the G1 phase. ConclusionsTaken together, our results suggested that CREB/TFDP3/E2F1 was involved in the pathogenesis of PCa. This provides novel insights into the mechanism of androgen-resistance in PCa.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%